Welcome

Welcome to the POZ/AIDSmeds Community Forums, a round-the-clock discussion area for people with HIV/AIDS, their friends/family/caregivers, and
others concerned about HIV/AIDS. Click on the links below to browse our various forums; scroll down for a glance at the most recent posts; or join in the
conversation yourself by registering on the left side of this page.

Privacy Warning: Please realize that these forums are open to all, and are fully searchable via Google and other search engines. If you are HIV positive
and disclose this in our forums, then it is almost the same thing as telling the whole world (or at least the World Wide Web). If this concerns you, then do not use a
username or avatar that are self-identifying in any way. We do not allow the deletion of anything you post in these forums, so think before you post.

The information shared in these forums, by moderators and members, is designed to complement, not replace, the relationship between an individual and his/her own
physician.

All members of these forums are, by default, not considered to be licensed medical providers. If otherwise, users must clearly define themselves as such.

Forums members must behave at all times with respect and honesty. Posting guidelines, including time-out and banning policies, have been established by the moderators
of these forums. Click here for “Am I Infected?” posting guidelines. Click here for posting guidelines pertaining to all other POZ/AIDSmeds community forums.

We ask all forums members to provide references for health/medical/scientific information they provide, when it is not a personal experience being discussed. Please
provide hyperlinks with full URLs or full citations of published works not available via the Internet. Additionally, all forums members must post information which are
true and correct to their knowledge.

I read over 1000 papers at the CROI 2007 in LA these look the most interesting to me...

this looks good... it says they are working on new powerful meds to wipe out the latent hiv cd4 cells...to try to get rid of hiv completely... it is a few steps ... look for more on.....Inhibitors of Histone Deacetylases HDAC) inhibitors

Background: Latently infected, resting memory CD4 T cells represent a major obstacle to eradication of HIV from infected individuals. Histone deacetylase (HDAC) inhibitors have been shown to induce viral expression from latently infected cells by changing chromatin structure at the integrated HIV promoter. We have tested 7 small-molecule HDAC inhibitors for their ability to block deacetylation of histones (H) 3 and 4 in primary CD4 T cells in vitro.

Methods: Uninfected primary CD4 cells were isolated from peripheral blood of healthy HIV-seronegative donors by negative selection. CD4 cells were treated with individual HDAC inhibitor at their highest tolerated dose (85% cell viability), and histone acetylation was assayed 4, 24, and 48 hours following treatment. Western blots of whole cell lysates were performed with acetylation-specific antibodies for H3 and H4, followed by stripping and re-probing with antibodies reactive to total histone. The ratio of acetylated to total H relative to the time 0 was used to compare the activity of the various compounds. Dose-response curves for each HDAC inhibitor were generated by treating primary CD4 cells with 10-fold dilutions over a 4-log range after 24 hours.

Results: All but 1 compound increased both H3 and, more dramatically, H4 acetylation. H3 and H4 acetylation increased 3- to 9- and 5- to 50-fold, respectively, until 24 hours after treatment, after which the response plateaued. Test compounds were more than twice as effective as valproic acid, a well-established HDAC inhibitor. At the highest tolerated dose, all 6 effective compounds were on the ascending slope of the dose-response curve.

Conclusions: The ability of several of the test compounds to increase H3 and, more dramatically, H4 acetylation is very encouraging in light of the fact that H4 acetylation is more directly associated with transcriptional control. The failure of 1 of the compounds, the only preferred class II HDAC inhibitor tested, to induce substantial acetylation, in contrast to the success of the other 4 class I specific and 2 nonselective HDAC inhibitors, suggests that class I HDAC may provide the best targets for viral induction from latency. Future studies will assess these compounds up to the maximum tolerated dose for the induction of HIV from our in vitro model of primary CD4 T-cell latency.

this one says... good news we found that if you are on HAART identifies" HIV+ DN T cells as the major producing infection.... ...HIV+ DN T cells is DN = CD4–CD8– (double negative, DN) so that may help with things...

Background: Peripheral blood mononuclear cell (PBMC)-associated viral RNA can be detected during all stages of HIV disease, including prolonged periods of successful ART. To assess its potential significance for HIV persistence, we dissected HIV-infected cells in PBMC according to their degree of viral transcriptional activity and their cellular phenotype.

Conclusions: Regardless of ART, the majority of HIV-infected cells harbor latent provirus engaged in basal viral transcription. Enhanced HIV transcription is associated with a DN phenotype rather than activation marker expression on CD4+ T cells. In conjunction with the phylogenetic proximity of CD4+ and DN T cell-derived quasispecies these findings provide strong in vivo evidence for CD4 down-modulation on HIV+ T cells during transition to productive infection. The abundance of viral RNA in PBMC-derived DN T cells from viremic patients and the almost complete absence of viral DNA and RNA in this cell type during ART identifies HIV+ DN T cells as the major phenotype for productive infection.